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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Specific erythroid-lineage defect in mice conditionally deficient for Mediator subunit Med1
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Specific erythroid-lineage defect in mice conditionally deficient for Mediator subunit Med1

机译:有条件地缺乏介体Med1亚基的小鼠中的特定类红系谱系缺陷

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摘要

The Mediator complex forms the bridge between transcriptional activators and the RNA polymerase II. Med1 (also known as PBP or TRAP220) is a key component of Mediator that interacts with nuclear hormone receptors and GATA transcription factors. Here, we show dynamic recruitment of GATA-1, TFIIB, Mediator, and RNA polymerase II to the β-globin locus in induced mouse erythoid leukemia cells and in an erythropoietin-inducible hematopoietic progenitor cell line. Using Med1 conditional knockout mice, we demonstrate a specific block in erythroid development but not in myeloid or lymphoid development, highlighted by the complete absence of β-globin gene expression. Thus, Mediator subunit Med1 plays a pivotal role in erythroid development and in β-globin gene activation.
机译:介体复合物形成转录激活剂和RNA聚合酶II之间的桥梁。 Med1(也称为PBP或TRAP220)是介体的关键组件,可与核激素受体和GATA转录因子相互作用。在这里,我们显示在诱导的小鼠类红细胞白血病细胞和促红细胞生成素诱导的造血祖细胞系中,将GATA-1,TFIIB,介体和RNA聚合酶II动态募集到β-球蛋白基因座。使用Med1条件性基因敲除小鼠,我们证明了类红细胞发育中的特定阻滞,但在髓样或淋巴样发育中却没有,具体表现为完全缺乏β-珠蛋白基因表达。因此,介体亚基Med1在红系发育和β-珠蛋白基因激活中起着关键作用。

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